The interdependence of function between the right (RV) and left (LV) ventricles is due to the close anatomical connections of the common muscle fibers in the free walls and the shared interventricular septum. Although most studies have been interested in diastolic interactions, in this grant we are concentrating on systolic interactions and hypothesize that RV systolic function is dependent on the LV for a sizeable fraction of its contractile force. This interaction can be quite important to the maintenance of RV function, not only in the normal heart, but during various disease conditions such as right heart failure or pulmonary hypertension, and during the use of left ventricular assist devices. Our goal is to determine the isolated systolic effects on RV function of instantaneously reducing left ventricular pressure in a single beat without changing RV or LV end-diastolic pressure or volume. The LV apex of anesthetized pigs will be connected to a prosthetic ventricle which is timed to fill immediately after diastole. Hearts will be studied from normal pigs and after heart failure is produced with our model of rapid ventricular pacing, which we have shown results in a realistic model of dilated congestive heart failure. Each heart will be instrumented for measurements of RV and LV chamber pressures with microtip catheters, instantaneous RV cardiac output with a pulmonary artery flow probe, and RV and LV septal-to-free wall dimensions with ultrasonic crystals. Data will be computer-sampled and a single unloaded beat will be compared to the preceeding steady-state normal beats, under conditions of varying preload and afterload, and with and without the pericardium. The LV to RV pressure gain (Gplr) and flow gain (Gflr) will be calculated as the instantaneous ratios of changes in RV pressure and pulmonary flow to change in LP pressure as a function of time during systole, and the stroke work gain (Grvsw) will be calculated as the integrated change in RV stroke work divided by integrated changes in LV pressure time integral. Our preliminary data demonstrate normalized (%/%) values of Gplr, Gflr, and Grvsw of 0.136, 0.237, and 0.513 in the normal heart, which means that 51% of the stroke work of the RV is due to the LV. Preliminary data from pigs in heart failure suggest that the gains are significantly higher (Grvsw=0.81) than in normal hearts. With these data we will confirm the hypothesis that up to 20% of RV systolic pressure is transmitted from the LV in the normal heart, and that the RV is even more dependent on LVP in congestive heart failure.